SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell-cell junctions

Vandewalle, Cindy

doi:10.1093/nar/gki965

Cited by 482 publications

(415 citation statements)

References 49 publications

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“…SCRIB complex is reciprocally inactivated by aPKC-dependent phosphorylation of Lgl protein. Vandewalle et al, 2005;Bermejo-Rodrı´guez et al, 2006;Moreno-Bueno et al, 2006;Peinado et al, 2007;Escrivaè t al., 2008). These different EMT regulators share a similar basic molecular mechanism of repression, binding to conserved E-box sequences (mainly of the CAGGTG type) in the proximal promoter of E-cadherin and other epithelial genes (Peinado et al, 2004(Peinado et al, , 2007.…”

Section: Regulation Of Cell Polarity Genes During Emtmentioning

confidence: 99%

Transcriptional regulation of cell polarity in EMT and cancer

2008

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The epithelial-to-mesenchymal transition (EMT) is a crucial process in tumour progression providing tumour cells with the ability to escape from the primary tumour, to migrate to distant regions and to invade tissues. EMT requires a loss of cell-cell adhesion and apical-basal polarity, as well as the acquisition of a fibroblastoid motile phenotype. Several transcription factors have emerged in recent years that induce EMT, with important implications for tumour progression. However, their effects on cell polarity remain unclear. Here, we have re-examined the data available related to the effect of EMT related transcription factors on epithelial cell plasticity, focusing on their impact on cell polarity. Transcriptional and post-transcriptional regulatory mechanisms mediated by several inducers of EMT, in particular the ZEB and Snail factors, downregulate the expression and/or functional organization of core polarity complexes. We also summarize data on the expression of cell polarity genes in human tumours and analyse genetic interactions that highlight the existence of complex regulatory networks converging on the regulation of cell polarity by EMT inducers in human breast carcinomas. These recent observations provide new insights into the relationship between alterations in cell polarity components and EMT in cancer, opening new avenues for their potential use as therapeutic targets to prevent tumour progression.

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Section: Regulation Of Cell Polarity Genes During Emtmentioning

confidence: 99%

Transcriptional regulation of cell polarity in EMT and cancer

2008

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“…As shown in Figures 6 and 7, Claudin-1 expression matched precisely that of E-cadherin in the ectoderm and neural epithelium, indicating that they are co-regulated during reorganization of junctional complexes occurring during neurulation. Of note, transcriptional regulators of E-cadherin, and notably Zeb-2, have also been shown to repress Claudin-1 expression in epithelial cells (Vandewalle et al, 2005).…”

Section: Expression Pattern Of Claudin-1 During Primary Neurulationmentioning

confidence: 99%

Timing and kinetics of E‐ to N‐cadherin switch during neurulation in the avian embryo

Dady

Blavet

Duband

2012

Developmental Dynamics

104

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Background: During embryonic development, cadherin switches are correlated with tissue remodelings, such as epithelium-to-mesenchyme transition (EMT). An E-to N-cadherin switch also occurs during neurogenesis, but this is not accompanied with EMT. The biological significance of this switch is currently unknown. Results: We analyzed the timing and kinetics of the E-to N-cadherin switch during early neural induction and neurulation in the chick embryo, in relation to the patterns of their transcriptional regulators. We found that deployment of the E-to N-cadherin switch program varies considerably along the embryonic axis. Rostrally in regions of primary neurulation, it occurs progressively both in time and space in a manner that appears neither in connection with morphological transformation of neural epithelial cells nor in synchrony with movements of neurulation. Caudally, in regions of secondary neurulation, neurogenesis was not associated with cadherin switch as N-cadherin pre-existed before formation of the neural tube. We also found that, during neural development, cadherin switch is orchestrated by a set of transcriptional regulators distinct from those involved in EMT. Conclusions: Our results indicate that cadherin switch correlates with the partition of the neurectoderm into its three main populations: ectoderm, neural crest, and neural tube.

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“…Western blot analysis showed that 30 days after radiation, tumors displayed significantly reduced E-cadherin expression, whereas E-cadherin expression maintained in the tumors of other two groups (Figure 5a). Furthermore, SIP1, an E-cadherin transcriptional repressor, 20 and TMPRSS4, which has been proved to induce EMT through ERK1/2 Figure 3 Effect of radiation on tumor regrowth, lung metastasis, intrahepatic dissemination and TMPRSS4 mRNA transcription. (a) The tumor regrowth was significantly inhibited 2 days after radiation (Po0.05), but recovered 30 days after radiation; (b) the incidence of lung metastasis from tumors 2 days after radiation was significantly inhibited (Po0.05), while that from tumors 30 days after radiation was significantly increased (Po0.05); (c) pathological examination showed that the intrahepatic dissemination was significantly increased after reimplantation of tumors 30 days after radiation (Po0.05); (d) quantitative RT-PCR analysis of TMPRSS4 days after radiation.…”

Section: Radiation-induced Epithelial-mesenchymal Transitionmentioning

confidence: 99%

Radiation enhances long-term metastasis potential of residual hepatocellular carcinoma in nude mice through TMPRSS4-induced epithelial–mesenchymal transition

Wang

et al. 2011

Cancer Gene Ther

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Recurrence and metastasis are frequently observed after radiotherapy for hepatocellular carcinoma (HCC), although upregulation of matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF) induced by radiation has been claimed to be involved, the mechanism is not clarified yet. In the present study, by using MHCC97L, a human HCC cell line with metastatic potential, and its xenograft in nude mice, we found that radiation induced a 48-to 72-h temporary increase in the expression of MMP-2 and VEGF both in vitro and in vivo, but only the in vitro invasiveness of MHCC97L cells was enhanced, while the in vivo metastatic potential of tumors was suppressed. Whereas, 30 days after radiation, when the expression of MMP-2 and VEGF decreased to unirradiated control levels, the in vivo dissemination and metastatic potential of residual tumors have just begun to increase with overexpression of TMPRSS4, which induced loss of E-cadherin through induction of Smad-Interacting Protein 1 (SIP1), an E-cadherin transcriptional repressor, and led to epithelial-mesenchymal transition (EMT). This process was blocked by treatment of siRNA-TMPRSS4. In conclusion, our study revealed novel findings regarding the biphasic effect of radiation on the metastatic potential of residual HCC. Overexpression of TMPRSS4 has a critical role in radiation-induced long-term dissemination and metastasis of residual HCC by facilitating EMT. These findings may provide new clues to suppress the radiation-induced dissemination and metastasis, thereby improve the prognosis of HCC patients.

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SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell-cell junctions

Cited by 482 publications

References 49 publications

Transcriptional regulation of cell polarity in EMT and cancer

Transcriptional regulation of cell polarity in EMT and cancer

Timing and kinetics of E‐ to N‐cadherin switch during neurulation in the avian embryo

Radiation enhances long-term metastasis potential of residual hepatocellular carcinoma in nude mice through TMPRSS4-induced epithelial–mesenchymal transition

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